literature

HIV mutation literature information.

HIV-1 drug resistance at antiretroviral treatment initiation in children previously exposed to single-dose nevirapine.

PMID: 21633285 2011 AIDS (London, England)

Result: Nineteen samples had major NRTI mutations, specifically K219E/Q (n=8), L74V (n=7), K70E (n=3), D67N (n=2) and L210W (n=1).

High prevalence of HIV-1 drug resistance among patients on first-line antiretroviral treatment in Lome, Togo.

PMID: 21663632 2011 Journal of the International AIDS Society

Result: Two patients had virus mutations indicative of the TAM-1 profile (M41L, L210W, T215S), and two of the TAM-2 profile (D67N, K70R, T215F, K219Q/R/E).

Table: L210W

Selection of HIV resistance associated with antiretroviral therapy initiated due to pregnancy and suspended postpartum.

PMID: 21765365 2011 Journal of acquired immune deficiency syndromes (1999)

Result: Several mutations associated with drug resistance that were not evaluated by OLA were detected by consensus sequencing, including M41L, V118I, E138A, and L210W.

Drug resistance patterns and virus re-suppression among HIV-1 subtype C infected patients receiving non-nucleoside reverse transcriptase inhibitors in South Africa.

PMID: 21927716 2011 Journal of AIDS & clinical research

Discussion: Among eight patients with TAMs, the most common pathway (seen in 6/8 patients) was TAM-2 related (D67N, K70R, K219Q/R/E); and the rest (2/8) were mixed with the TAM-1 pathway (M41L, L210W, T215Y) extending similar prior Southern African observations.

A structural frame for understanding the role of thymidine analogue resistance mutations in resistance to zidovudine and other nucleoside analogues.

PMID: 22024508 2011 Antiviral therapy

Abstract: These mutations, known as thymidine analogue resistance mutations (TAMs) are M41L, D67N, K70R, L210W, T215F/Y and K219E/Q.

Increase of transmitted drug resistance among HIV-infected sub-Saharan Africans residing in Spain in contrast to the native population.

PMID: 22046345 2011 PloS one

Result: Both specimens harboured mutations F53L and L90M at PR and M41L, K103N, L210W and T215D at RT.

Phenotypic analysis of HIV-1 genotypic drug-resistant isolates from China, using a single-cycle system.

PMID: 22047156 2011 Molecular diagnosis & therapy

Abstract: The phenotype results showed that individual pseudoviruses with four thymidine analog mutations (TAMs).[M41L, T67N, L210W, and T215Y] in combination with various other mutations had different levels of resistance to nucleoside reverse transcriptase inhibitors (NRTIs).

Resistance patterns selected by nevirapine vs. efavirenz in HIV-infected patients failing first-line antiretroviral treatment: a bayesian analysis.

PMID: 22132100 2011 PloS one

Introduction: With regard to subtype, in subjects infected with HIV-1 subtype B, the thymidine analogue mutations pathway 1 or TAM-1 (including mutations M41L, L210W and T215Y) is probably more frequent t

Discussion: Our analysis offers strong evidence that, in contrast to the mutation patterns published for other subtypes, individuals infected with CRF01_AE and experiencing virologic failure while receiving NVP-based HAART favor TAM-2 resistance pathways (K70R, D67N, T215F, K219Q/E) rather than TAM-1 (M41L, L210W, T215Y), whereas those receiving regimens containing EFV appear to select both TAM-2 and TAM-1 pathways (Figures 1B, 2A and 3B).

Emerging trends of drug-resistant HIV-1 among drug-treated patients in former blood donors in Hubei, China: a three-year surveillance from 2004 to 2006.

PMID: 22160938 2011 Virologica Sinica

Abstract: Genotypic drug resistance analysis showed significant increases in percentages of patients carrying HIV-1 strains with M41L, T215Y/F, D67N, K103N, G190A/S, Y181C/F or L210W mutations.

Does GSS still maintain relevance on HAART outcome after the introduction of newest active antiretroviral drugs? 48 weeks results.

PMID: 22211659 2011 Current HIV research

Abstract: Data also showed a > 60% recurrence of specific mutations for NRTI: M41L, M184IV, L210W, T215FY, K219EQ and 75% for D67N.

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